It is apparent from reports in the literature that PFK from liver controls glycolysis and also is involved in concert with FDPase in the control of gluconeogenesis. There are four possible mechanisms by which PFK may regulate metabolism. These are: (a) conformational changes induced by ligands, (b) association-dissociation properties, (c) protein-protein interaction with other cytoplasmic proteins, and (d) physiological chemical modification. In this proposal we plan to study the molecular regulatory mechanisms of pig liver PFK, FDPase and PFK-stabilizing factor by correlating enzyme kinetic data from protein-protein interaction studies with physico-chemical interaction studies by the use of Light Scattering Techniques. Since it has not been established that the protein-protein interaction of PFK-FDPase is of physiological significance, we propose to study another possible mechanism of regulation of glycolysis and gluconeogenesis. These studies will involve the investigation of the presence of PFK-kinase and PFK-phosphatase in pig liver which are reported to yield active PFK and inactive PFK, respectively, in rat liver. These mechanisms could explain the rapid rates of gluconeogenesis under conditions of nutritional stress and the effects of hormones such as glucagon, which has been shown to decrease the assayable activity of rat liver PFK.